Trauma is the leading cause of death in Americans between the ages of one and forty years. Shock lung, the pulmonary insufficiency that can follow severe trauma and shock, is a major cause of death in patients who are initially successfully resuscitated from their injuries. The objective of this proposal is to analyze the role of arachidonic acid metabolites (including the native prostaglandins) in the pathogenesis of shock lung. The work will be done in the Staub sheep preparation. This preparation is unique in that it allos access to pure pulmonary lymph. The lymph flows and lymph composition will provide insight into lung fluid dynamics and, moreover, will allow assay of arachidonic acid metabolites in a representative of lung interstitial fluid, i.e. in lung lymph. The sheep will be subjected to a combined hemorrhagic-septic insult. Metabolism of arachidonic acid will then be studied. The study should yield information about: (1) the pulmonary metabolism of arachidonic acid; (2) the physiological and pathophysiological responses of the lung to arachidonic acid metabolites at the microvascular level in vivo in the unanesthetized animal, and (3) the relationship of arachidonic acid metabolites and shock lung, at least in the experimental animal.